Non-vascular complications of diabetes Flashcards

1
Q

What populations are most likely to develop a hyperosmolar hyperglycemic state (HHS)?

A

Occurs almost exclusively in Type 2 DM, elderly and physically impaired or limited access to free water

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2
Q

What distinguishes HHS from DKA?

A

Severe hyperglycemia >600, Hyperosmolality. Develops more insidiously with polyuria, polydipsia, and weight loss several days before hospital admission. Greater degree of dehydration

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3
Q

What are the causes of hyperosmolar hyperglycemic state (HHS)?

A

Catabolic Stress, Insufficient intake of water, Excessive water loss, High sugar intake, Drugs

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4
Q

What are the clinical presentations of hyperosmolar hyperglycemic state (HHS)?

A

polyuria, polydipsia, weight loss, vomiting, tachycardia, hypotension, severe dehydration, seizures, hyperthermia

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5
Q

What are the lab findings of hyperosmolar hyperglycemic state (HHS)?

A

Blood glucose > 600. Serum osmolality >320. Serum Na+ - normal to high (135-145). Serum K+ - normal (4-5). Serum Bicarb >20. pH > 7.3. Ketones – negative. Complicated by thromboembolic events

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6
Q

What is the treatment of DKA and HHS?

A

medical emergencies. IV fluid and electrolyte replacement. Slower rate and greater volume needed for HHS. Insulin replacement starts after rehydration is in progress

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7
Q

How does HHS and DKA differ clinically?

A

to the presence of ketoacidosis and the degree of hyperglycemia

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8
Q

What diabetic population is hypoglycemia more common?

A

type 1 diabetes, Type 1’s suffer an average of 2 episodes of symptomatic hypoglycemia per week.

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9
Q

What are the causes of hypoglycemia?

A

Insulin injections, Oral hypoglycemic agents, Gastroparesis, Hepatic and renal dysfunction, Malnutrition

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10
Q

What are the neurogenic symptoms associated with a hypoglycemica episode?

A

catecholamine-mediated/adrenergic: Tremor, palpitations, and anxiety/arousal. acetylcholine-mediated/cholinergic: sweating, hunger, and paresthesias

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11
Q

What are the neuroglycopenic symptoms associated with a hypoglycemic episode?

A

cognitive impairment, behavioral changes, psychomotor abnormalities, seizure and coma

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12
Q

What are the cardiovascular signs associated with a hypoglycemic episode?

A

diaphoresis, pallor, tachycardia, HTN

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13
Q

What causes absent of symptoms of hypoglycemia?

A

Loss of autonomic warning due to recent antecedent hypoglycemia, prior exercise, or sleep. Autonomic neuropathy due to diminished epi response. Medications like beta-blockers

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14
Q

What is the criteria for a hypoglycemic coma and how is it treated?

A

Unconsciousness lasting more than 30 minutes after plasma glucose is corrected. IV mannitol (40 g as a 20% solution over 20 minutes). Glucocorticoids (e.g., dexamethasone, 10 mg)

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15
Q

What is the dawn phenomenon?

A

high morning blood glucose between 5-9am due to the release of counter-regulatory hormones (cortisol, GH, glucagon)

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16
Q

What is the Somogyi Effect?

A

Rebound Hyperglycemia—Iatrogenic, low sugars in the middle of the night, high sugars in the morning

17
Q

How do you determine whether an early morning high blood sugar level is caused by dawn phenomenon or Somogyi effect?

A

check blood sugar levels around 2 a.m. to 3 a.m. for several nights. If the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi effect. If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it’s likely the dawn phenomenon

18
Q

What defines hypoglycemia in patients without diabetes?

A

Whipple’s triad: signs and symptoms of hypoglycemias, plasma glucose <60, and resolution of those signs/symptoms after raising plasma glucose

19
Q

What is factitious hypoglycemia?

A

occurs secondary to the secret use of insulin. plasma insulin is high while C-peptide is low. This applies to nondiabetic patients and those with type II DM, not type I diabetics who always have low C-peptide levels

20
Q

What is included in the triad of DKA?

A

hyperglycemia, anion gap metabolic acidosis, and ketonemia